title: Wnt signaling in caudal dysgenesis and diabetic embryopathy.
abstract: BACKGROUND
  Congenital defects are a major complication of diabetic pregnancy, and the leading cause of infant death in the first year of life. Caudal dysgenesis, occurring up to 200-fold more frequently in children born to diabetic mothers, is a hallmark of diabetic pregnancy. Given that there is also an at least threefold higher risk for heart defects and NTDs, it is important to identify the underlying molecular mechanisms for aberrant embryonic development.
  
  
  METHODS
  We have investigated gene expression in a transgenic mouse model of caudal dysgenesis, and in a pharmacological model using situ hybridization and quantitative real-time PCR.
  
  
  RESULTS
  We identified altered expression of several molecules that control developmental processes and embryonic growth.
  
  
  CONCLUSIONS
  The results from our models point towards major implication of altered Wnt signaling in the pathogenesis of developmental anomalies associated with embryonic exposure to maternal diabetes.
authors.affiliation: Department of Pediatrics, University of Nebraska Medical Center, Omaha, Nebraska, USA.
authors.forename: Gabriela
authors.initials: G
authors.lastname: Pavlinkova
authors.forename: J Michael
authors.initials: JM
authors.lastname: Salbaum
authors.forename: Claudia
authors.initials: C
authors.lastname: Kappen
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000196:embryology* / Q000235:genetics; D004195:Disease Models, Animal; D004622:Embryo, Mammalian / Q000378:metabolism; D005260:Female; D005315:Fetal Diseases / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D008822:Mice, Transgenic; D009436:Neural Tube Defects / Q000209:etiology* / Q000378:metabolism; D011247:Pregnancy; D011254:Pregnancy in Diabetics; D015398:Signal Transduction; D051153:Wnt Proteins / Q000235:genetics / Q000378:metabolism*
chemical_list: D051153:Wnt Proteins